We read with great interest the article by Mayer et al1 dealing with the relationship between inflammatory status and long-term mortality in 1065 patients with asymptomatic carotid atherosclerosis. The results of their study demonstrated that the risk of all-cause and cardiovascular mortality significantly increased in patients with elevated serum levels of high-sensitivity C-reactive protein (CRP). In addition, patients with a high degree of carotid atherosclerosis and increased high-sensitivity CRP levels were particularly at risk of adverse outcome. The authors further showed that the individual extent of atherosclerosis and inflammatory status might jointly predict long-term mortality. The authors proposed that measurement of high-sensitivity CRP in combination with ultrasound investigations of the carotid arteries at a single time point could provide additional prognostic information for patients with asymptomatic carotid atherosclerosis.

Evidence indicates that impaired endothelial function may strongly be related to carotid atherosclerosis. Bai et al2 demonstrated that in the meta-analysis of 22 studies with 6168 subjects, the levels of asymmetrical dimethylarginine (an endogenous nitric oxide synthase inhibitor) were positively related to carotid intima–media thickness, especially in patients with chronic kidney disease. In a study presented previously, we showed that carotid intima–media thickness might be significantly associated with increased levels of plasma asymmetric dimethylarginine in hypertensive subjects.3 On the contrary, it was demonstrated that the plasma high-sensitivity CRP levels were inversely correlated with plasma nitric oxide metabolites in hypertensive men.4 Zoccali et al5 proposed that in patients undergoing hemodialysis with initially normal intima–media thickness, asymmetric dimethylarginine and CRP were interacting factors in the progression of carotid intimal lesions, suggesting a possible link between asymmetric dimethylarginine and inflammation in carotid atherosclerosis.5

In this context, it is strongly speculated that elevated inflammatory status might be accompanied by the impaired nitric oxide bioavailability and endothelial dysfunction. Therefore, we would like to know whether the increased levels of inflammatory status and carotid stenosis might be linked to the impaired endothelial function in the study of Mayer et al.1 Further studies should be performed to assess more precisely the relationships among inflammatory status, endothelial dysfunction, and carotid stenosis and their prognostic value for the development of cardiovascular diseases in patients with asymptomatic carotid atherosclerosis.

Kazushi Tsuda, MDCardiovascular and Metabolic Research CenterKansai University of Health SciencesOsaka, Japan

Disclosures

None.

Footnotes

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